Under controlled experimental conditions, CO is associated with excellent agreement and good trending ability when compared with the gold standard CO. In the paediatric clinical setting, CO performs well; by contrast, CO, an operator- and anatomy-dependent technology, appears less reliable than CO.

Fourteen critically ill neonatal and paediatric intensive care patients with various primary diagnoses and signs of associated pulmonary hypertension received inhaled nitric oxide (NO), 20-80 ppm, after failure of conventional therapy to improve oxygenation. NO administration was found to be associated with a significant improvement in postductal arterial oxygen tension (pre-NO: 3.75 (SD 1.39) kPa; post-NO: 6.05 (SD 1.70) kPa; p = 0.004). In 10 patients, NO was found to increase arterial oxygen tension with more than 1 kPa. In 2 of these patients, ECMO treatment could be avoided due to the pronounced improvement in gas exchange seen after the initiation of NO administration. The remaining 4 patients failed to respond to NO administration. One patient developed methaemoglobinaemia (13.9%) which required treatment with methylthionine. Since we were unable to produce any beneficial effect of NO in the late phase of the pulmonary disease process, we believe that, in order to be successful, inhaled NO should be instituted when conventional treatment has failed and the administration of an iv vasodilator is usually considered.

No abstract

Left ventricular output was measured non-invasively at predefined time intervals from less than 15 minutes to 72 hours after birth in 16 infants who had been born at full term. The blood flow velocity in the ascending aorta was measured by a range gated Doppler technique and multiplied by the cross sectional diameter measured by cross sectional and M mode echocardiography. Left ventricular output remained high in the first two hours, 235-243 ml/min/kg, despite a 10% decrease in heart rate. The fall in heart rate was compensated for by a 15% increase in stroke volume. Between 2 and 24 hours there was a significant fall in mean (SD) left ventricular output to 187 (35) ml/min/kg caused mainly by a reduction in stroke volume. The fall in left ventricle output after two hours may reflect an adaptation to the decreased demand on the left ventricle as the ductus constricts.